Search for: [Abstract = "Gastrointestinal dysfunction is one the most critical non\-motor features of Parkinsonʼs disease \(PD\) and may not only constitute the initial clinical feature but also occur long before typical PD symptomatology. The impairment of the enteric nervous system in the pathogenesis of PD has already been suggested. Even a slight damage or change in activity of myenteric neurons may cause considerable gut dysmotility, malabsorption and disrupted excretion. Various exogenous toxins,may cross the intestinal barrier, initiate neurodegeneration processes in enteric nervous system and subsequently in the central nervous system. The aims of the study were\: firstly, to measure the long\-term influence of salsolinol on morphometric parameters of the myenteric ganglia and subclasses of motoneurons in the Wistar rat jejunum, secondly, to evaluate the long\-term effects on regulatory ICC and thirdly, to measure gastrointestinal motility \(stomach emptying, intestinal transit and colonic motility\) and to roughly assess the mechanism of neurotoxic action of salsolinol. It occurs salsolinol might mediate neuronal cell death by initiation of apoptosis. Impairment of myeteric plexus neurons, especially the subclass of inhibitory motor neurons \(nitrergic\), might be responsible for sustained smooth muscle contraction and may lead to delayed gastric emptying together with abnormal colonic motility. Thus, salsolinol may be considered as useful substance to induce experimental parkinsonism."]

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